As a society we come to terms with things and sometimes it takes the questioning and critically thinking involved in science to change what society has assumed to be true. The consumption of ethanol has always been looked at for its negative effects; however, with the ever-growing fascination of drugs and alcohol scientists like Dr. Collins have discovered fascinating things in regards to ethanol's contribution to prevention.
Michael Collins et al. wrote the article Moderate Ethanol Preconditioning of Rat Brain Cultures Engenders Neuroprotection Against Dementia-Inducing Neuroinflammatory Proteins: Possible Signaling Mechanisms that focuses on ethanol preconditioning that provides neuroprotection against neuroinflammatory proteins that induce dementia. Although previous studies have been conducted about ethanol and some of its heart benefits, Collins et al. have done some new studies with regards to its positive benefits in neuroprotection for memory related diseases. What I find particularly interesting is how ethanol preconditioning has shown to increase pro inflammatory mediators such as reactive oxygen species like superoxides. These mediators induce neuroprotection from toxins that cause aging, like beta-amyloid.
In a related study Ethanol preconditioning protects against ischemia/reperfusion-induced brain damage: Role of NADPH oxidase-derived ROS by Qun Wang et al. used ethanol preconditioning in gerbils to see if it provided neuroprotective effects for people with cerebral ischemia. He, too, found there to be neuroprotective effects when ethanol consumption triggered reactive oxygen species (e.g. superoxides) produced by NADPH oxidase.
It appears that ethanol preconditioning triggers NADPH oxidase to produce these reactive oxygen species, which then are involved in neuroprotection; more specifically they effect cellular function including stimulation of kinases and pro-inflammatory genes (as pointed out in NADPH Oxidases, Reactive Oxygen Species, and Hypertension: Clinical implications and therapeutic possibilities by Tamara Paravicini and Rhian Touyz), which is seen in both examples of moderate ethanol preconditioning. This is astounding because there are effects linked to NADPH oxidase and many cellular functions that reactive oxygen species control, and to be able to induce a reaction via ethanol preconditioning could potentially help many other diseases.
According to Paravicini and Touyz, reactive oxygen species are involved in hypertentsion, atherosclerosis, diabetes, and chronic kidney disease. With the implications of the work done by Collins et al. and Wang et al., these diseases may be affected by moderate ethanol preconditioning as well.
The discovery of ethanol preconditioning truly may lead to many more discoveries of various treatments for diseases like diabetes, cerebral ischemia, and Alzheimer's disease, and also might provoke research for ethanol substitutes.
Works Cited
Collins, Michael A. et al. "Moderate Ethanol Preconditioning of Rat Brain Cultures Engenders Neuroprotection Against Dementia-Inducing Neuroinflammatory Proteins: Possible Signaling Mechanisms." Molecular neurobiology 41.2-3 (2010): 420-425. PMC. Web. 16 Oct. 2015.
Paravicini, Tamara M., PHD, and Rhian M. Touyz, MD, PHD. "NADPH Oxidases, Reactive Oxygen Species, and Hypertension Clinical Implications and Therapeutic Possibilities." Diabetes Care 31 (2008): S170-180. American Diabetes Association. Web. 15 Oct. 2015.
Wang, Qun et al. "Ethanol preconditioning protects against ischemia/reperfusion-induced brain damage: Role of NADPH oxidase-derived ROS." Free radical biology & medicine 43.7 (2007): 1048-1060. PMC. Web. 16 Oct. 2015.
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